Can the development of atrial fibrillation in patients with ischemic heart failure with low ejection fraction be predicted?

OBJECTIVE: Our aim is to determine the triggering factors of paroxysmal atrial fibrillation (PAF) in ischemic heart failure (HF) patients with low ejection fraction (EF). METHODS: Sixty patients were included in this study. Echocardiography and 24-hours Holter monitoring were performed after measurement of serum NT-pro BNP concentration. The patients were classified into two groups concerning the occurrence of PAF on Holter recordings. Biochemical and echocardiographic parameters of patients with and without PAF were compared. RESULTS: PAF was detected in 28 (46%) patients. Patients with PAF demonstrated higher NT-pro BNP levels, mitral and aortic regurgitation velocities, E/A, E/E', pulmonary capillary wedge pressure, pulmonary artery systolic pressure, left atrial volume and volume indices. NT-pro BNP was established as the predictor of PAF (OR=1.23, 95% CI: 1.08-1.42; p=0.001). ROC analysis showed an NT-pro BNP value of 2188 pg/mL as cut-off value with 68% sensitivity and 84% specificity [Area under the ROC curve (AUC)=0.826, CI 95%: 0.724-0.927; p<0.001]. CONCLUSION: The triggering factors for AF are increased intracardiac pressures, left atrial dilatation and increased wall tension. As an indicator of increased wall tension, elevated levels of NT-pro BNP predict the development of PAF.

Serum neurokinin B levels in newly diagnosed nondipper hypertensive patients.

OBJECTIVE: Cardiovascular diseases are more common in patients with nondipper hypertension (NDHT) compared with those with dipper hypertension (DHT). The aim of this study is to evaluate the serum neurokinin B levels in DHT and NDHT patients. METHODS: The study population included newly diagnosed hypertensive patients who were not under antihypertensive treatment. A total of 77 patients were evaluated with ambulatory blood pressure monitoring and divided into two groups: NDHT (n=42) and DHT (n=35). Plasma neurokinin B levels were measured using the ELISA method. RESULTS: Serum neurokinin B levels were significantly higher in the NDHT group compared with the DHT group [254 (180-888) and 207 (116-752) pg/ml, respectively; P=0.024]. There is a positive correlation between the mean night-time systolic blood pressure and plasma neurokinin levels (r=0.590; P<0.001). On regression analysis, neurokinin B level was only found to be related to the mean night-time systolic blood pressure (unstandardized ß=-22.02±9.59; P<0.001). CONCLUSION: Plasma neurokinin B level is higher in patients with NDHT, indicating an unfavorable cardiovascular prognosis. There is a need for further studies that search for the relation between serum neurokinin B levels and NDHT.

Characterization of the apelin -1860T>C polymorphism in Turkish coronary artery disease patients and healthy individuals.

To evaluate the association between the apelin -1860T>C polymorphism and plasma apelin levels in Turkish patients with coronary artery disease (CAD). A total of 276 individuals were enrolled in the present study, including 158 patients with CAD and 118 individuals without CAD as controls. The presence of the apelin -1860T>C gene polymorphism and plasma apelin levels were determined using polymerase chain reaction/restriction fragment length polymorphism and enzyme-linked immunosorbent assay, respectively. Significance was set at p≤0.05 for all statistical analyses. The genotype and allele frequencies of interested genes were significantly different between groups (χ(2)=10.2; df=2; p=0.006 and χ(2)=13.4; df=1; p=0.000, respectively). Frequency of CC genotype and the C allele of -1860T>C site was significantly higher in CAD patients compared to healthy controls. We found that individuals with the TC and CC genotypes were associated with an increased risk of CAD when compared with the TT genotype in CAD patients, and the adjusted ORs (95% CI) were 6.50 (1.27-33.0) and 6.39 (1.77-23.0), respectively. Plasma apelin levels were significantly lower in CAD patients compared to control group. Apelin level of CAD patient group having CC genotype of -1860T>C site was significantly lower compared to those having TT genotypes, but it was not statistically significant (p > 0.05). The homozygous CC genotype of apelin gene is associated with high risk of CAD. Apelin gene polymorphism -1860T>C is a significant predictor of predisposition to CAD in in Turkish population.

APJ receptor A445C gene polymorphism in Turkish patients with coronary artery disease.

Coronary artery disease (CAD) is a disease in which a waxy substance called plaque builds up inside the coronary arteries. Apelin is a novel endogenous peptide with inotropic and vasodilatory properties and is the ligand for the angiotensin receptor-like 1 (APJ) receptor. We aimed to determine genotype and allele frequencies of APJ receptor A445C gene polymorphism in Turkish patients with CAD and healthy controls by RFLP-PCR. This study was performed on 159 unrelated CAD patients and 62 healthy controls. We obtained AA, AC and CC genotype frequencies in CAD patients as 41.5%, 49.1% and 9.4%, respectively. In the control group, frequencies of genotypes were found as 35.5% for AA, 48.4% for AC and 16.1% for CC. We did not observe difference in APJ receptor A445C polymorphism between CAD patients and healthy controls (χ(2) = 2.178; df = 2; P = 0.336). The A allele was encountered in 66% (210) of the CAD and 59.7% (74) of the controls. The C allele was seen in 34% (108) of the CAD and 40.3% (50) of the controls. Allele frequencies of interested genes were not significantly different between groups (χ(2) = 1.57; df = 1; p = 0.225). The frequencies of APJ receptor A445C genotype were not significantly different between control and patients. None of the three APJ receptor A445C genotypes, AA, AC and CC displayed significant difference in CAD patients. We did not find any difference in the clinical parameters except for weight and diastolic blood pressure levels in the AA, AC and CC genotypes of patients. Individuals with CC genotypes had significantly higher weight, systolic and diastolic blood pressure levels and systolic blood pressure than other genotypes, P ≤ 0.05. In addition, HDL-C level was found decreased, but this reduction was not statistically significant. Contrarily, the low levels of weight, SBP, DBP and TC were statistically significant in the subjects with AA genotype in CAD. In conclusion, CC genotype carriers may have more risk than other genotypes in the development of hypertension in CAD, but not AAgenotype carriers. We suggest that this polymorphism may not be a marker of CAD, but it may cause useful in function of the apelin/APJ system and may be a genetic predisposing factor for diagnostic processes and can be helpfull in finding new treatment strategies. We think that it is required to further comprehensive studies in order to make clear this situation in CAD.